In the first cycle of this P01, our collective and synergistic efforts have clearly established the validity of our central hypothesis that "excessive TGFB signaling plays a key role in the pathobiology of the neonatal chronic lung injury termed BPD". The logical extension of these findings "what's upstream and downstream of TGF in chronic neonatal lung injury and are there any useful therapeutic targets in this pathway?" is a key question that will be the focus of this revised renewal application. Thus, we propose a research program to address the following 5 inter-related, mutually reinforcing and synergistic aspects of this key question. Project 1. Warburton and Gauldie. Excess TGFB in neonatal lung injury and repair. Project 2. Minoo. BPD: interactions between inflammation and morphogenesis. Project 3. Derynck. Non-Smad mechanisms of TGFB signaling Project 4. Groffen. Negative regulation of lung inflammation by Abr/Bcr. Project 5. Bellusci. FGFR2b pathway in Bronchopulmonary Dysplasia.